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10.1007/s13311-014-0292-z http://scihub22266oqcxt.onion/10.1007/s13311-014-0292-z C4391382!4391382!25005000     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25005000&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Neurotherapeutics 2014 ; 11 (4): 721-31 Nephropedia Template TP {{tp|p=25005000|t=2014. Repeat-Associated Non-AUG Translation and Its Impact in Neurodegenerative Disease |pdf=|usr=}}{{25005000}} gab.com Text Repeat-Associated Non-AUG Translation and Its Impact in Neurodegenerative Disease JO: Neurotherapeutics http://www.kidney.de/pget.php?&tw=1&pmid=25005000 #FOAvip Nucleotide repeat expansions underlie numerous human neurological disorders. Repeats can trigger toxicity through multiple pathogenic mechanisms, including RNA gain-of-function, protein gain-of-function, and protein loss-of-function pathways. Traditionally, inference of the underlying pathogenic mechanism derives from the repeat location, with dominantly inherited repeats within transcribed noncoding sequences eliciting toxicity predominantly as RNA via sequestration of specific RNA binding proteins. However, recent findings question this assumption and suggest that repeats outside of annotated open reading frames may also trigger toxicity through a novel form of protein translational initiation known as repeat-associated non-AUG (RAN) translation. To date, RAN translation has been implicated in 4 nucleotide repeat expansion disorders: spinocerebellar ataxia type 8; myotonic dystrophy type 1 with CTG?CAG repeats; C9orf72 amyotrophic lateral sclerosis/frontotemporal dementia with GGGGCC?GGCCCC repeats; and fragile X-associated tremor/ataxia syndrome with CGG repeats. RAN translation contributes to hallmark pathological characteristics in these disorders by producing homopolymeric or dipeptide repeat proteins. Here, we review what is known about RAN translation, with an emphasis on how differences in both repeat sequence and context may confer different requirements for unconventional initiation. We then discuss how this new mechanism of translational initiation might function in normal physiology and lay out a roadmap for addressing the numerous questions that remain.Electronic supplementary material: The online version of this article (doi:10.1007/s13311-014-0292-z) contains supplementary material, which is available to authorized users. Twit Text FOAVip Repeat-Associated Non-AUG Translation and Its Impact in Neurodegenerative Disease ????Neurotherapeutics http://www.kidney.de/pget.php?&tw=1&pmid=25005000 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25005000 #FOAvip English Wikipedia <ref>{{Cite pmid|25005000}}</ref> Repeat-Associated Non-AUG Translation and Its Impact in Neurodegenerative Disease #MMPMID25005000 Kearse MG; Todd PK Neurotherapeutics 2014[Oct]; 11 (4): 721-31 PMID25005000show ga Nucleotide repeat expansions underlie numerous human neurological disorders. Repeats can trigger toxicity through multiple pathogenic mechanisms, including RNA gain-of-function, protein gain-of-function, and protein loss-of-function pathways. Traditionally, inference of the underlying pathogenic mechanism derives from the repeat location, with dominantly inherited repeats within transcribed noncoding sequences eliciting toxicity predominantly as RNA via sequestration of specific RNA binding proteins. However, recent findings question this assumption and suggest that repeats outside of annotated open reading frames may also trigger toxicity through a novel form of protein translational initiation known as repeat-associated non-AUG (RAN) translation. To date, RAN translation has been implicated in 4 nucleotide repeat expansion disorders: spinocerebellar ataxia type 8; myotonic dystrophy type 1 with CTG?CAG repeats; C9orf72 amyotrophic lateral sclerosis/frontotemporal dementia with GGGGCC?GGCCCC repeats; and fragile X-associated tremor/ataxia syndrome with CGG repeats. RAN translation contributes to hallmark pathological characteristics in these disorders by producing homopolymeric or dipeptide repeat proteins. Here, we review what is known about RAN translation, with an emphasis on how differences in both repeat sequence and context may confer different requirements for unconventional initiation. We then discuss how this new mechanism of translational initiation might function in normal physiology and lay out a roadmap for addressing the numerous questions that remain.Electronic supplementary material: The online version of this article (doi:10.1007/s13311-014-0292-z) contains supplementary material, which is available to authorized users. äRepeat-Associated Non-AUG Translation and Its Impact in Neurodegenerat(epmc).pdf DeepDyve Pubget Overpricing